FIGURE 6.

Inhibition of solTNF prevents ANGII-induced AAA expansion. (A) Representative macroscopic images showing AAA expansion in vehicle (saline) or XPro1595 (2 mg/kg) ANGII-infused Apoe^–/– mice. (B) Representative ultrasound images of the abdominal aorta at its maximal inner circumference at day 0 and day 28 of the ANGII-induced AAA from vehicle-treated and XPro1595-treated mice. (C) ANGII-induced AAA expansion assessed by inner abdominal aortic circumference. (D) The percentage change in the maximal inner abdominal aortic circumference from day 0 to day 28 in vehicle- and XPro1595-treated mice assessed by ultrasound€ (E) Ex vivo-measured maximal outer aortic diameter in the two groups. (F) Ex vivo-measured surface area of the AAA treated with vehicle and XPro1595. (G) Representative micrographs of AAA cross-sections stained with Miller’s elastin stain (black) in vehicle- and XPro1595-treated AAAs. Arrows point to rupture of elastic fibers. (H) Medial elastin degradation semi-quantified by a 4-grade system in aneurysms from XPro1595- and vehicle-treated mice. (I) MMP-9 immunoreactivity in cross-sections of vehicle- and XPro1595-treated aneurysms and the representative semi-quantification (number of positive cells/mm²). Black arrowheads indicate positive stained cells. IgG isoform was used as negative control. Results are shown as mean SEM if data passed the D’Agostino and Pearson omnibus normality tests. Mann–Whitney test was applied in D and presented as median with interquartile range as data were non-normally distributed. *Denotes p < 0.05 analyzed by unpaired student t-test for two-group comparison or two-way ANOVA with Bonferroni test for multiple comparisons. Contingency table data in H was analyzed by Fisher exact probability test with Freeman-Halton extension. Outliers were identified by Grubb’s outlier test for normally distributed data and indicated by red squares () and excluded from the statistical analyses. M, media; Ad, adventitia.